At the end of Decmber 1993 and also at the end ofJanuary 1995, the rer Meuse, one of the maeor s in Eurpe, flooded and. river bank were inundated. We i ted the possible health risks of exposure to heairy metal conentrations i river bank soils ul om the floodig of the iver Meus at the ead of 1993. Soil

A human health risk assessment has been performed in relation to recreational activities on two artificial freshwater lakes along the river Meuse in The Netherlands. Although the discharges of contaminants into the river Meuse have been reduced in the last decades, which is reflected in decreasing concentrations of pollutants in surface water and suspended matter, the levels in sediments are more persistent. Sediments of the two freshwater lakes appear highly polluted and may pose a health risk in relation to recreational activities. To quantify health risks for carcinogenic (e.g., polycyclic aromatic hydrocarbons) as well as noncarcinogenic compounds (e.g., heavy metals), an exposure assessment model was used. First, we used a standard model that solely uses data on sediment pollution as the input parameter, which is the standard procedure in sediment quality assessments in The Netherlands. The highest intake appeared to be associated with the consumption of contaminated fish and resulted in a health risk for Pb and Zn (hazard index exceeded 1). For the other heavy metals and for benzo(a)pyrene, the total averaged exposure levels were below levels of concern. Secondly, input data for a more location-specific calculation procedure were provided via analyses of samples from sediment, surface water, and suspended matter. When these data (concentrations in surface water) were taken into account, the risk due to consumption of contaminated fish decreased by more than two orders of magnitude and appeared to be negligible. In both exposure assessments, many assumptions were made that contribute to a major degree to the uncertainty of this risk assessment. However, this health risk evaluation is useful as a screening methodology for assessing the urgency of sediment remediation actions.ImagesFigure 1Figure 2Figure 3

The foetus is exposed to multiple xenobiotics through the mother's circulation and this is possibly involved in the development of diseases in later life. Heavy metals and lipophilic genotoxins in umbilical cord blood of newborns may have synergistic effects on mutagenesis in the hypoxanthine-phosphoribosyltransferase (HPRT) reporter gene. Concentrations of zinc (Zn), lead (Pb) and cadmium (Cd) were determined in the peripheral and cord blood of 16 non-smoking and 9 smoking healthy mothers by atomic absorption spectrometry. Lipophilic DNA adducts in lymphocytes were determined in the same subjects by 32P-postlabelling and the HPRT-variant frequency was assessed by the evaluation of 6-thioguanine resistant cells. Although the Cd/Zn ratio was 2.5-fold higher in the blood of smoking women than in non-smoking women (1.0 +/- 0.2 and 0.4 +/- 0.1, respectively, P = 0.007), this difference could not be observed in umbilical cord blood (0.3 +/- 0.1 and 0.3 +/- 0.1, respectively, P = 0.66). Similarly, mean DNA adduct levels were increased in the lymphocytes of smoking women compared with non-smoking controls (0.99 +/- 0.31 adducts/10(8) nt and 0.43 +/- 0.12, respectively, P = 0.009), but were only marginally higher in the neonates of smokers than in their non-smoking counterparts (0.57 +/- 0.29 and 0.24 +/- 0.09, respectively, P = 0.38). Since Cd is known to effectively inhibit DNA repair, we hypothesized that concomitant exposure of neonates to Cd and genotoxic compounds may result in an increased fixation of DNA damage into somatic mutations. Indeed, the number of HPRT-variants per adduct (i.e. the mutagenic efficiency of adducts) correlated positively with the Cd concentrations in cord blood (r = 0.61, P = 0.001). These data suggest a molecular link between DNA damage, inhibition of DNA repair by Cd and in vivo mutagenesis during foetal development. Thus, exposure to heavy metals may enhance the mutagenic potential of DNA-damaging compounds and results in biologically relevant genotoxic effects in neonates.

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In recent years, several studies have addressed a possible relationship benteen nitrate exposure and childhood type 1 insulin-dependent diabetes meilitus. The present ecologic study describes a possible relation between the incidence of type 1 diabetes and nitrate levels in drinking water in The Netherlands, and evaluates whether the World Health Organization and the European Commission stndard for nitrate in drinking water (50 mg/L) is adequate to prevent risk of this disease. During 1993During -1995 Even though experimental data raise serious concern about the formation of Nnitroso compounds and carcinogenic risk, the epidemiologic evidence for an association between the intake of nitrate and cancer is regarded to be insufficient. Therefore, the World Health Organization (WHO) guideline value for nitrate in drinking water (50 mg/L nitrate units as nitrate ion) was established solely to prevent methemoglobinemia (6). In the European Union, the maximum admissible nitrate level in drinking water was also set at 50 mg/L (A). In a recent review on the role of drinking water nitrate as a cause of infantile methemoglobinemia (7), it was concluded that the standard of 50 mg/L might be unnecessarily strict and that gastrointestinal infection and inflammation and the ensuing overproduction of nitric oxide may be the cause of infantile methemoglobinemia attributed to drinking water nitrate (8). In our view, however, rather than raising the standard of nitrate to levels > 50 mg/L, other adverse health effects of nitrate exposure should be taken into consideration. We suggest that the present drinking water guideline value for nitrate of 50 mg/L needs to be reconsidered for multiple reasons. Even though the guideline value is aimed at the protection of infants as the highest risk group against methemoglobinemia, cases of methemoglobinemia as a result of exposure to nitrate in drinking water < 50 mg/L have been reported (59. In a previous study (1), we observed increased hprt variant frequencies in lymphocyte DNA of subjects who used private well water with nitrate levels below the guideline value of 50 mg/L as drinking water. Also, formation of the carcinogenic N-nitrosodimethylamine was observed during uptake of nitrate at the acceptable daily intake level-corresponding with the standard of nitrate in drinking water-in combination with nitrosatable